No abstract

[³H]PK 11195 binding to the peripheral benzodiazepine binding site was investigated in the brain and liver of mice treated with ethanol (4 g/kg, p.o.) daily for 5 days. In the brain stem, B_max was decreased by 78% in the ethanol-treated group with unaltered K_d (2 nM). The ethanol-withdrawn group did not differ from the control group in both parameters. In the cerebellum, B_max was decreased by 74% but the binding affinity increased 5-fold as the K_d decreased from 10 to 2 nM. The ethanol-withdrawn group did not differ significantly from the ethanol-treated group. No changes were observed in the cerebrum and liver. These results further support the idea that [³H]PK 11195 binding may be a useful marker for ethanol consumption. The observed changes in these binding sites may represent a functional adaptive response to the ethanol insult and/or a role in the mediation of the effects of ethanol.